Alzheimer's disease (AD) is the most common cause of dementia, affecting tens of millions of individuals worldwide. Neuritic plaques are accumulations of aggregated amyloid beta (Aβ) peptides, including Aβ1-40 and Aβ1-42, derived from processing of amyloid precursor protein (APP) by β- and γ-secretases. The vast majority of autosomal familial AD (FAD)-linked mutations are associated with increased levels of Aβ1-42, providing strong evidence that Aβ1-42 plays a central role in AD pathogenesis. There are currently no effective therapies for arresting or reversing the impairment of cognitive function that characterizes AD. There is a need in the art for effective therapies for treating AD and related disorders.